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Essentials of Diagnosis

General Considerations

Metabolic alkalosis is an acid–base disorder in which a primary disease process leads to the net accumulation of base within or the net loss of acid from the extracellular fluid (ECF). When it occurs as a simple acid–base disorder, it is recognized as an increase in plasma [HCO3−] and a compensatory increase in arterial blood pH.

Unopposed by other primary acid–base disorders, the increase in arterial blood pH promptly and predictably depresses ventilation resulting in increased Paco2 and buffering of the magnitude of the alkalemia; an increase in Paco2 of 0.6–0.7 mm Hg for every 1.0 mEq/L increase in plasma [HCO3−] is predicted from empirical studies. Although a Paco2 greater than 55 mm Hg is uncommon, compensatory increases to 60 mm Hg or higher have been documented in severe metabolic alkalosis. The magnitude of the compensatory increase in Paco2 is directly related to the extent of the alkalosis and the degree of elevation of the plasma [HCO3−], whether or not there is an intracellular acidosis. This compensatory respiratory response is independent of hypoxia, hypokalemia, renal failure, and cause and is usually not detectable clinically because it is more dependent on a change in depth rather than the rate of ventilation.

The major clinically and pathophysiologically relevant classification is based on whether the metabolic alkalosis is dependent on Cl− depletion. The Cl−-depletion forms, also termed the Cl−-responsive alkaloses, are more common. The other major grouping is the Cl−-resistant alkaloses, most of which are due to K+ depletion with mineralocorticoid excess. Mixed K+ and Cl−-depletion metabolic alkaloses also occur. Several other relatively uncommon causes constitute the balance of etiologies of metabolic alkalosis (Table 5–1).